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LGD-4033 (Ligandrol, VK5211) is a non-steroidal selective androgen receptor modulator (SARM) laboratory grade chemical reagent with HPLC purity ≥98%, with confirmation of identity by mass spectrometry and a certificate of analysis (COA) for each batch. The material is delivered in capsule form, solely as a raw material for research work.
Chemical reagent intended exclusively for laboratory tests (Research Use Only). It is not a medicinal product, dietary supplement or food. It is not intended for administration to humans or animals outside a controlled experimental environment.
LGD-4033, also known by its common name Ligandrol and development code VK5211, is non-steroidal selective androgen receptor modulator (SARM). The “LGD” code comes from Ligand Pharmaceuticals – the company in whose laboratories the molecule was created. Viking Therapeutics then took over the rights to further develop the compound, giving it the internal designation VK5211 and working on its application in the context of losing muscle mass in patients during convalescence. The three designations – LGD-4033, Ligandrol, VK5211 – refer to the same molecule and appear interchangeably in the literature.
LGD-4033’s place in overall development SARM class described in a review by Narayanan, Coss, and Dalton (2018). The authors reconstruct the path from the first non-steroidal androgen receptor ligands, through arylpropionamide molecules, to compounds with diverse chemical cores – including pyrrolidine-benzonitrile derivatives, which include LGD-4033. The common theme of this work was the search for a ligand that would maintain the anabolic effect on muscles and bone, and at the same time limit the stimulation of androgenic tissues, such as the prostate. This research goal—not any validated therapeutic effect—defines the purpose of the entire class.
LGD-4033 is among the best characterized members of the class next to ostarine (MK-2866). It is distinguished by a published Phase I study involving healthy young men (Basaria 2013), which is a unique rather than typical situation within SARMs – most compounds from this family have not received peer-reviewed clinical data at all. However, it is worth pointing out the proportions right away: a single phase I study is the earliest stage of evaluating a molecule, and not proof of effectiveness or safety in the long term.
In research, LGD-4033 functions as a laboratory reagent – a raw material for in vitro work and research on animal models conducted by qualified units. It is not a substance with the status of a medicine, dietary supplement or food. No regulatory institution has approved LGD-4033 for sale as a product intended for human use.
| Parameter | Value |
|---|---|
| Common name | Ligandrol |
| Development codes | LGD-4033 / VK5211 |
| Relationship class | Nonsteroidal SARM (selective androgen receptor modulator) |
| CAS number | 1165910-22-4 |
| Summary formula | C₁₄H₁₂F₆N₂O |
| Molar mass | ~338.25 g/mol |
| Origin | Ligand Pharmaceuticals → Viking Therapeutics |
| Form | Capsules (substance content declared in batch documentation / COA) |
| Storage conditions | A dry, cool place, away from light and moisture; original packaging |
| Cleanliness | HPLC >=98% |
| Identity confirmation | Mass spectrometry (MS) |
| Documentation | COA for each batch, batch traceability |
| Destiny | For laboratory testing only (RUO) |
| WADA status | List of prohibited substances, category S1 (anabolic agents) |
The structure of the molecule is based on a pyrrolidine-benzonitrile core with fluorine substituents. The presence of six fluorine atoms in the molecule has direct analytical significance: the fluorinated fragment gives a characteristic fragmentation pattern in mass spectrometry, which facilitates both the control of the identity of the research material and the detection of the compound in anti-doping analysis. The non-steroidal nature of the core – the lack of the four fused ring system typical of steroids – is the most important structural difference from steroid androgens and the starting point for understanding the mechanism.
The androgen receptor (AR) belongs to the nuclear receptor superfamily and functions as a ligand-activated transcription factor. Its structure is modular. The N-terminal domain is responsible for most of the transcriptional activity and constitutes a platform for interactions with regulatory proteins. The DNA-binding domain recognizes specific sequences in the promoters of target genes. The ligand-binding domain forms a pocket in which the androgen molecule — or, in the case of SARMs, a non-steroidal molecule — settles.
The sequence of events is as follows: the ligand enters the binding domain pocket, the receptor changes conformation, the chaperones detach, the receptor moves to the cell nucleus, dimerizes and binds to DNA regulatory sequences. This stage alone does not determine the effect. The next step – the recruitment of accessory proteins – determines whether gene expression is enhanced or silenced. Coactivators, including the SRC/p160 family, enhance transcription; corepressors suppress it.
This is the essence of tissue selectivity. The shape of the receptor–ligand complex is not identical for each molecule: different ligands stabilize slightly different conformations of the binding domain. A different conformation means different affinity for coactivators and corepressors. Because the profile of available accessory proteins differs in muscle, bone and prostate tissue, the same ligand may induce different transcriptional responses in them. Narayanan (2018) and Solomon (2019) describe this model as the theoretical basis of the SARM class – with the caveat that it is a model reconstructed from preclinical data and not a simple principle transferable to any organism.
The difference is mechanistic, not marketing. Testosterone and anabolic-androgenic steroids are substrates of two enzymes of great physiological importance. The first of them, 5α-reductase, converts testosterone into dihydrotestosterone (DHT) – an androgen with a stronger affinity for AR, largely responsible for the effect on the prostate, skin and hair follicles. The second, aromatase, converts androgens to estrogens, including testosterone to estradiol.
LGD-4033, as a non-steroidal molecule, does not have a steroid core recognized by these enzymes. It is not a substrate of either 5α-reductase or aromatase. This means that LGD-4033 does not produce DHT or estradiol in the body – the entire charge of the interaction remains at the level of direct binding to the androgen receptor (Narayanan 2018, Solomon 2019).
The conclusion may be overinterpreted, so it is worth closing it precisely. The lack of enzymatic conversion does not mean no effect on the endocrine system. Direct activation of the androgen receptor triggers feedback in the hypothalamus-pituitary-gonadal axis, which in a phase I study resulted in a reduction in endogenous testosterone concentration (Basaria 2013). Different metabolic pathway, same regulatory loop.
In preclinical data, LGD-4033 is described as a ligand with high affinity for the androgen receptor, showing anabolic effects on muscle and bone tissue in animal models with relatively weaker stimulation of androgenic tissues, such as the prostate (Solomon 2019). It is this disparity between tissues that provides the operational definition of “selectivity” in the class name.
Selectivity is sometimes reported as an anabolic-androgenic ratio – a number that compares the response of muscle tissue to the response of prostate tissue. In a critical review of the class, Bond (2025) draws attention to how this parameter can be overused. The value depends on the animal model, the chosen endpoint, the measurement method and the exposure range at which the comparison was made. It is not a physical constant of the molecule that can be specified to a decimal place and transferred to another species. Numbers circulating non-scientifically as alleged “anabolic factors” of SARMs are not supported by peer-reviewed literature.
The authors of the critical review go further: they emphasize that the translation of selectivity observed in rodents into predictable, reproducible effects in humans remains unproven, and the evidence base for the entire SARM class has significant methodological gaps (Bond 2025). The mechanism is therefore well described at the molecular level – but poorly characterized at the level of long-term physiological consequences.
The only published human clinical trial for this compound remains the work of Basaria and colleagues (2013). It is worth discussing it together with the structure of the study, because without this context its results may be exaggerated.
Research design. This was a randomized, double-blind, placebo-controlled study conducted in healthy young men. Participants received the compound orally for a short period of time, with increasing levels of exposure in subsequent groups. Endpoints included pharmacokinetic parameters, safety indicators, and hormonal response.
What was reported. The authors reported oral bioavailability – the compound is absorbed from the gastrointestinal tract, which distinguishes it from many peptides requiring a different route of administration. Pharmacokinetics were linear in the tested exposure range, and the half-life was long, on the order of 24 hours. There was also an exposure-dependent reduction in endogenous testosterone concentration, which disappeared after the end of exposure – the suppression was therefore reversible over the observed time horizon.
Limitations. A Phase I trial, by definition, answers questions about tolerability and pharmacokinetics, not efficacy. The sample was small, the follow-up time was short, the population was narrow (healthy young men – not elderly people, not women, not patients). Functional endpoints were missing: the study did not assess muscle strength, performance or hard clinical outcomes. A short horizon does not allow detection of rare events or distant effects. The results of this study are data on the substance obtained under strictly controlled experimental conditions – they do not constitute product characteristics or grounds for any use outside the laboratory.
The following list organizes the available literature by model, endpoint and evidentiary value.
Basaria (2013) – Phase I, people. Design: healthy young men, randomization, placebo, double blinding. Endpoints: pharmacokinetics, short-term safety, hormonal response. Reported: oral bioavailability, linear pharmacokinetics, long half-life, reversible suppression of endogenous testosterone, decrease in HDL cholesterol fraction. Limitations: small sample, short time, lack of functional endpoints.
Narayanan, Coss, Dalton (2018) – review paper. Model: Synthesis of preclinical and early clinical data for the entire class. Endpoint: medicinal chemistry and mechanism reconstruction. Reported: history of SARM development, molecular basis of tissue selectivity, lack of conversion to DHT and estradiol as a distinguishing feature from steroid androgens. Limitation: The review does not generate new data and conclusions about selectivity are based primarily on rodent models.
Solomon (2019) – state of the art review. Model: literature review, SARM class. Endpoint: Summary of potential clinical directions and safety signals. Reported: no approval of any SARM for clinical use, repeatable signals of effects on the hormonal axis and lipid profile. Limitation: heterogeneity of sources, lack of data from high-powered studies.
Bond (2025) – Critical Review. Model: A critical assessment of the classroom evidence base. Endpoint: reliability of reported parameters and knowledge gaps. Reported: dependence of the anabolic-androgenic ratio on the model and method, lack of long-term data, discrepancy between the image of SARMs in non-scientific circulation and the state of the literature. Limitation: the study does not provide new primary data – it organizes existing data.
Leciejewska (2024) – class adverse events. Model: review of reports of adverse events associated with the use of SARMs. Endpoint: nature and frequency of events reported. Reported: repeated reports of liver dysfunction, hormonal axis suppression and lipid changes. Limitation: data comes largely from reports and case reports, with no population denominator.
Labban (2024) – DILI case report. Model: single clinical case. Endpoint: drug-induced liver injury associated with LGD-4033. Reported: hepatotoxicity in a person exposed to the compound. Limitation: The case report cannot estimate frequency or establish causality with certainty – but it documents a real signal.
Van Wagoner (2017) – Internet product analytics. Model: chemical analysis of preparations sold online as SARMs. Endpoint: content matches the label. Reported: extensive discrepancies between declaration and actual composition. Constraint: market sample from a specific period.
Thevis and Schänzer (2018) – anti-doping analytics. Model: detection methodology. Endpoint: detection of SARMs and their metabolites. Reported: effective LC-MS/MS methods.
Joshi (2025) – Social Media Analysis. Model: Exploration of self-reported side effects in content published by people using SARMs. Endpoint: catalog of reported complaints. Limitation: self-reported data, without medical verification, subject to selection error – signaling value, not evidential value.
What we don’t know. LGD-4033 has no Phase III trials. There are no large, long-term studies with hard endpoints. The evidence base for this molecule is clearly narrower than for ostarine – even though LGD-4033 is considered one of the better-studied SARMs. This sentence accurately reflects the scale: “better studied” in this class means a single Phase I study, not a registration program.
A reliable description of the reagent includes safety signals reported in the literature. The information below concerns the chemical itself and comes from scientific research – it does not constitute product characteristics or information about its use.
Suppression of the hypothalamic-pituitary-gonadal axis. In a phase I study, an exposure-dependent reduction in endogenous testosterone concentration was observed, which disappeared after discontinuation of the compound (Basaria 2013). The mechanism is a direct consequence of androgen receptor activation and feedback in the hormonal axis. Reversibility was observed in the short study horizon – data on the recovery of hormonal parameters after longer exposures do not exist.
Changes in the lipid profile. The decrease in the HDL cholesterol fraction is described as a class effect – it has been reported for both LGD-4033 and other SARMs (Basaria 2013, Solomon 2019, Leciejewska 2024). The direction of change is unfavorable from the point of view of cardiovascular risk assessment, and its significance in chronic exposure remains unknown.
Impact on hematological parameters. Activation of the androgen receptor is associated with the stimulation of erythropoiesis, which translates into an increase in hematocrit – a phenomenon known from research on androgens and signaled in studies regarding the SARM class (Solomon 2019).
Drug-induced liver injury (DILI). Labban and colleagues (2024) published a case report of drug-induced liver injury associated with LGD-4033. This is a single clinical report, so it does not allow us to estimate the frequency of the phenomenon or establish a causal relationship with full certainty. However, it documents a real signal of hepatotoxicity – a signal that is confirmed in the broader picture of adverse events reported for the entire class (Leciejewska 2024). This is one of the most important pieces of information in the safety profile of this compound and remaining silent about it would be dishonest.
Self-reported data. Joshi and colleagues (2025) analyzed content posted on social media by people using SARMs, cataloging the reported ailments. This type of material has limited evidentiary value: there is no medical verification, no confirmation of the identity of the substance, no control and no population denominator. It should be treated as a signal indicating directions for further research, not as evidence.
No long-term data. Bond (2025) emphasizes that the full safety profile of the SARM class remains uncharacterized. There are no studies covering long-term exposure, no data on long-term effects, and no safety assessment in populations other than healthy young men.
LGD-4033 is on the World Anti-Doping Agency (WADA) List of Prohibited Substances and Methods. category S1 – anabolic agents. The ban is in force at any time: both during and beyond the launch period. This applies to all SARMs as a class, regardless of the form of packaging and the declared purpose of the material.
Anti-doping analytics has proven tools for detecting these compounds. Thevis and Schänzer (2018) describe methods based on liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) that detect both the parent molecule and its metabolites in urine. The fluorinated core of LGD-4033 produces a distinctive fragmentation pattern that facilitates clear identification. The long half-life of the compound and the presence of metabolites translate into a wide detection window – the signal in the sample remains detectable long after exposure ceases.
Cross-contamination is a separate issue. Van Wagoner’s (2017) analysis showed that preparations sold online as SARMs are sometimes contaminated with other compounds – including substances from the prohibited list. People working in the sports environment should be aware that contact with analytically uncontrolled material carries analytical risks beyond the declared identity of the substance.
The reagent is supplied in capsule form. The capsule is only a form of packaging research material – portioning into repeatable units facilitates batch registration and analytical work.
The capsule form does not change the status of the reagent. Packaging into capsules is a technical solution, not a suggestion of intended use. LGD-4033 remains a Research Use Only chemical reagent it is not intended for consumption by humans or animals.
It is worth stating this rule directly, because it can be a source of misunderstandings: character is not a regulatory class. The legal status of a substance is determined by the substance itself and its marketing authorization, not the shape of the packaging. The same molecule in the capsule and in the vial falls under exactly the same Research Use Only framework. The capsule does not make the reagent a dietary supplement, just as the vial does not make it a medicine.
The substance content in the unit and its purity are confirmed by the batch analytical documentation (COA). The material is stored in its original packaging, in a dry and cool place, away from light and moisture; capsule form does not require a cold chain. Work with the reagent should be carried out in accordance with the internal procedures of the research unit and be carried out by qualified personnel.
LGD-4033 is available in the European Union only as a research reagent (Research Use Only). Relationship it is not registered by the European Medicines Agency (EMA) or the American FDA as a medicinal product. It is also not authorized as a food or dietary supplement ingredient – no SARM has obtained such status in any jurisdiction.
In the context of sports, the compound is on the WADA List of Prohibited Substances and Methods category S1 (anabolic agents) — as a prohibited substance at all times. These facts constitute an element of a reliable description of the relationship and are important for the awareness of people working in a sports environment.
A fair description of a research reagent requires that the limits of knowledge be stated as clearly as the limits of knowledge itself.
What is LGD-4033?
LGD-4033 (Ligandrol, VK5211) is a non-steroidal selective androgen receptor modulator (SARM) – a chemical reagent intended for laboratory research only. CAS number: 1165910-22-4.
Is LGD-4033 a drug or dietary supplement?
NO. The compound does not have EMA or FDA registration as a medicinal product and is not authorized as a food or dietary supplement ingredient. It is a research reagent (Research Use Only), not intended for consumption.
How does LGD-4033 differ from an anabolic steroid?
Structure and metabolism. LGD-4033 does not have a steroid core, so it is not a 5α-reductase or aromatase substrate – it does not produce DHT or estradiol (Narayanan 2018, Solomon 2019). This does not mean hormonal neutrality: direct activation of the androgen receptor triggers feedback in the hypothalamic-pituitary-gonadal axis (Basaria 2013).
What was reported in the Phase I trial?
Basaria (2013) – a randomized, double-blind, placebo study in healthy young men – reported oral bioavailability, linear pharmacokinetics, long half-life and a reversible reduction in endogenous testosterone concentration and HDL fraction. The study was short, with a small sample size and no functional endpoints.
What is known about the effects of LGD-4033 on the liver?
A case report of drug-induced liver injury (DILI) associated with LGD-4033 has been published (Labban 2024). A single report does not allow estimating the frequency of the phenomenon, but it documents a real signal of hepatotoxicity – consistent with the broader picture of adverse events reported for the SARM class (Leciejewska 2024).
Is LGD-4033 detectable in doping control?
Yes. LC-MS/MS methods detect both the parent molecule and its metabolites; a long half-life translates into a wide detection window (Thevis, Schänzer 2018).
Is LGD-4033 banned in sports?
Yes. The association is listed on the WADA List in the category S1 (anabolic agents) — as a prohibited substance at any time, including outside the starting period.
Why do HPLC purity and COA matter?
Chemical analysis of products sold online as SARMs showed that a significant part of them did not contain the declared substance, some contained other compounds, and the content often differed from the label (Van Wagoner 2017). Without confirmation of purity (HPLC), identity (MS) and batch affiliation (COA), the material is not suitable for scientific work.
Does a capsule mean it’s a supplement?
NO. The character is not a regulatory class. The capsule is only a form of packaging; the same substance in the capsule and in the vial falls under the same Research Use Only framework and is not intended for consumption.
How to store the reagent?
In the original packaging, in a dry and cool place, away from light and moisture – in accordance with the batch documentation and internal procedures of the research facility. The capsule form does not require a cold chain.
Are there phase III studies of LGD-4033?
NO. The union did not pass the registration program. Available clinical data are limited to Phase I, and the long-term safety profile remains uncharacterized (Bond 2025).
How is LGD-4033 different from ostarine (MK-2866)?
These are two separate compounds from the same class, with different chemical cores. Ostarine has a broader evidence base – including data from larger studies. One phase I study has been published for LGD-4033 (Basaria 2013), so its evidence base is clearly narrower. Both compounds are listed on the WADA List in Category S1 and both remain research reagents.
What is the difference between LGD-4033, Ligandrol and VK5211?
Nothing – these are three designations of the same molecule. LGD-4033 is the laboratory code of Ligand Pharmaceuticals, Ligandrol is the common name, VK5211 is the designation assigned by Viking Therapeutics.
More in the knowledge base: the LGD-4033 (Ligandrol) category and a profile article on LGD-4033.
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